Vulnerability to tuberculosis in patients with HIV: a viral protein implicated
According to the World Health Organisation, tuberculosis is the cause of death in one in three cases of people living with HIV. In fact, HIV-positive individuals are 15 to 30 times more likely to contract tuberculosis, even when receiving effective antiretroviral treatment.
In a study published in the journal PLOS Pathogens, a research team1 led by a CNRS scientist highlights the key role played by the viral protein Tat22, secreted by HIV-infected cells, in this phenomenon of hyper-vulnerability. Among the researchers is David Perrais, from the IINS.
Studies conducted on human cells and zebrafish larvae have revealed that this viral protein blocks the cell defence mechanism known as autophagy, thereby promoting the survival and multiplication of the bacterium Mycobacterium tuberculosis – responsible for tuberculosis – in target cells3.
These findings shed new light on the synergy between HIV and tuberculosis and pave the way for the development of innovative therapeutic strategies. Although the Tat protein remains difficult to target at present, treatments aimed at restoring the autophagy mechanism could be developed to better protect patients.
- From the Montpellier Infectious Diseases Research Institute (CNRS/University of Montpellier), the Laboratory of Pathogens and Host Immunity (CNRS/Inserm/University of Montpellier), the Institute of Pharmacology and Structural Biology (CNRS/University of Toulouse) and the Interdisciplinary Institute of Neuroscience (CNRS/University of Bordeaux).
- Transactivator of transcription.
- Called macrophages, these cells belong to the white blood cell group, and their main role is to destroy cellular debris and pathogens throughout the body.
Reference
HIV-1 Tat favors the multiplication of Mycobacterium tuberculosis and toxoplasma by inhibiting clathrin-mediated endocytosis and autophagy. A. Rivault, A. Bernut, M. Ben-Neji, M. Abrantes, M. Jansen, S. Huc-Brandt, S. Besteiro, Y. Bordat, N. Audemard, M. Mesleard-Roux, D. Perrais, O. Neyrolles, G. Lugo-Villarino, C. Vérollet, L. Espert et B. Beaumelle. PLOS Pathogens, 18 september 2025.
https://doi.org/10.1371/journal.ppat.1013183